The present research has demonstrated that environmental stressors acting during prenatal but not postnatal periods of sexual differentiation feminize and demasculinize the sexual behavior potentials of male rats. Assays of fetal testosterone levels indicate that the primary mechanism inducing the prenatal stress syndrome appears to be a hyposecretion of the primary gonadal androgen, testosterone, during critical stages of fetal development. The male fetuses of mothers stressed during the third trimester pregnancy, show increased plasma testosterone titers on Day 17 of gestation followed by markedly decreased testosterone on Day 18. Normal males exhibit peak testosterone titers on Day 18 of gestation. A series of experiments are now in progress. These are designed to delineate further the alterations in sexually dimorphic behaviors characteristic of prenatally stressed male rats and to identify in more detail the mechanism mediating the syndrome.